The following is a summary of “Mucosal neuroimmune mechanisms in gastroesophageal reflux disease (GERD) pathogenesis,” published in the January 2024 issue of Gastroenterology by Leech, et al.

Gastro-esophageal reflux disease (GERD) presents as chronic visceral pain in the distal esophagus and is commonly treated with proton pump inhibitors (PPIs). However, a significant portion of patients are unresponsive to PPI therapy, and prolonged use may have adverse effects. Recent findings suggest nerve fiber density and distribution play integral roles in oesophageal nociception in GERD patients. Additionally, alterations in oesophageal mucosal cells, including epithelial cells, mast cells, dendritic cells, and T lymphocytes, have been extensively studied in GERD. Chronic acidic reflux in GERD induces macro- and micro-inflammation in the oesophageal epithelium.

In gastrointestinal conditions like irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD), bidirectional interactions between immune cells and mucosal nerve fibers contribute to pathogenesis and symptom generation. Inflammatory processes in these conditions drive sensory alterations, such as nerve fiber outgrowth and hypersensitivity, leading to visceral pain signaling.

The study aimed to explore the molecular pathways linking inflammation and sensory perception in GERD symptom development. Furthermore, it investigated analogous mechanisms in other gastrointestinal regions, such as IBS and IBD, which may shed light on novel avenues for GORD research.

Reference: link.springer.com/article/10.1007/s00535-023-02065-9